Reduction of oxidative stress by carvedilol: role in maintenance of ischaemic myocardium viability
To differentiate the impact of the beta-blocking and the anti-oxidant activity of carvedilol in maintaining myocardium viability. Isolated rabbit hearts, subjected to aerobic perfusion, or low-flow ischaemia followed by reperfusion, were treated with two doses of carvedilol, one dose (2.0 microM) wi...
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| Veröffentlicht in: | Cardiovascular research 2000-08, Vol.47 (3), p.556-566 |
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| container_title | Cardiovascular research |
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| creator | CARGNONI, A CECONI, C BERNOCCHI, P BORASO, A PARRINELLO, G CURELLO, S FERRARI, R |
| description | To differentiate the impact of the beta-blocking and the anti-oxidant activity of carvedilol in maintaining myocardium viability.
Isolated rabbit hearts, subjected to aerobic perfusion, or low-flow ischaemia followed by reperfusion, were treated with two doses of carvedilol, one dose (2.0 microM) with marked negative inotropic effect due to beta-blockage and the other (0.1 microM) with no beta-blockage nor negative inotropism. Carvedilol was compared with two doses of propranolol, 1.0 - without - and 5.0 microM - with negative inotropic effect. Anti-oxidant activity was measured as the capacity to counteract the occurrence of oxidative stress and myocardium viability as recovery of left ventricular function on reperfusion, membrane damage and energetic status.
Carvedilol counteracted the ischemia and reperfusion induced oxidative stress: myocardial content of reduced glutathione, protein and non-protein sulfhydryl groups after ischaemia and particularly after reperfusion, was higher in hearts treated with carvedilol, while the myocardial content of oxidised glutathione was significantly reduced (0.30+/-0.03 and 0.21+/-0.02 vs. 0.39+/-0.03 nmol/mg prot, both P |
| doi_str_mv | 10.1016/s0008-6363(00)00082-1 |
| format | Article |
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Isolated rabbit hearts, subjected to aerobic perfusion, or low-flow ischaemia followed by reperfusion, were treated with two doses of carvedilol, one dose (2.0 microM) with marked negative inotropic effect due to beta-blockage and the other (0.1 microM) with no beta-blockage nor negative inotropism. Carvedilol was compared with two doses of propranolol, 1.0 - without - and 5.0 microM - with negative inotropic effect. Anti-oxidant activity was measured as the capacity to counteract the occurrence of oxidative stress and myocardium viability as recovery of left ventricular function on reperfusion, membrane damage and energetic status.
Carvedilol counteracted the ischemia and reperfusion induced oxidative stress: myocardial content of reduced glutathione, protein and non-protein sulfhydryl groups after ischaemia and particularly after reperfusion, was higher in hearts treated with carvedilol, while the myocardial content of oxidised glutathione was significantly reduced (0.30+/-0.03 and 0.21+/-0.02 vs. 0.39+/-0.03 nmol/mg prot, both P<0.01, in 0.1 and 2.0 microM). At the same time, carvedilol improved myocardium viability independently from its beta-blocking effect. On the contrary, propranolol maintained viability only at the higher dose, although to a lesser extent than carvedilol. This suggests that the effects of propranolol are dependent on energy saving due to negative inotropism. The extra-protection observed with carvedilol at both doses is likely due to its anti-oxidant effect.
Our data show that the anti-oxidant activity of carvedilol is relevant for the maintenance of myocardium viability.</description><identifier>ISSN: 0008-6363</identifier><identifier>EISSN: 1755-3245</identifier><identifier>DOI: 10.1016/s0008-6363(00)00082-1</identifier><identifier>PMID: 10963728</identifier><identifier>CODEN: CVREAU</identifier><language>eng</language><publisher>Oxford: Oxford University Press</publisher><subject>Adenosine Diphosphate - metabolism ; Adenosine Triphosphate - metabolism ; Adrenergic beta-Antagonists - therapeutic use ; Analysis of Variance ; Animals ; Antianginal agents. Coronary vasodilator agents ; Antioxidants - therapeutic use ; Biological and medical sciences ; Carbazoles - therapeutic use ; Cardiovascular system ; Carvedilol ; Dose-Response Relationship, Drug ; Male ; Medical sciences ; Myocardial Reperfusion Injury - prevention & control ; Myocardium - metabolism ; Oxidative Stress - drug effects ; Perfusion ; Pharmacology. Drug treatments ; Phosphocreatine - metabolism ; Propanolamines - therapeutic use ; Propranolol - therapeutic use ; Rabbits ; Random Allocation</subject><ispartof>Cardiovascular research, 2000-08, Vol.47 (3), p.556-566</ispartof><rights>2000 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c447t-bfe7a55574ee3960f9d998b158066494976a142903bd00f79ee6792f6987d5e33</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,781,785,27929,27930</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1462100$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10963728$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>CARGNONI, A</creatorcontrib><creatorcontrib>CECONI, C</creatorcontrib><creatorcontrib>BERNOCCHI, P</creatorcontrib><creatorcontrib>BORASO, A</creatorcontrib><creatorcontrib>PARRINELLO, G</creatorcontrib><creatorcontrib>CURELLO, S</creatorcontrib><creatorcontrib>FERRARI, R</creatorcontrib><title>Reduction of oxidative stress by carvedilol: role in maintenance of ischaemic myocardium viability</title><title>Cardiovascular research</title><addtitle>Cardiovasc Res</addtitle><description>To differentiate the impact of the beta-blocking and the anti-oxidant activity of carvedilol in maintaining myocardium viability.
Isolated rabbit hearts, subjected to aerobic perfusion, or low-flow ischaemia followed by reperfusion, were treated with two doses of carvedilol, one dose (2.0 microM) with marked negative inotropic effect due to beta-blockage and the other (0.1 microM) with no beta-blockage nor negative inotropism. Carvedilol was compared with two doses of propranolol, 1.0 - without - and 5.0 microM - with negative inotropic effect. Anti-oxidant activity was measured as the capacity to counteract the occurrence of oxidative stress and myocardium viability as recovery of left ventricular function on reperfusion, membrane damage and energetic status.
Carvedilol counteracted the ischemia and reperfusion induced oxidative stress: myocardial content of reduced glutathione, protein and non-protein sulfhydryl groups after ischaemia and particularly after reperfusion, was higher in hearts treated with carvedilol, while the myocardial content of oxidised glutathione was significantly reduced (0.30+/-0.03 and 0.21+/-0.02 vs. 0.39+/-0.03 nmol/mg prot, both P<0.01, in 0.1 and 2.0 microM). At the same time, carvedilol improved myocardium viability independently from its beta-blocking effect. On the contrary, propranolol maintained viability only at the higher dose, although to a lesser extent than carvedilol. This suggests that the effects of propranolol are dependent on energy saving due to negative inotropism. The extra-protection observed with carvedilol at both doses is likely due to its anti-oxidant effect.
Our data show that the anti-oxidant activity of carvedilol is relevant for the maintenance of myocardium viability.</description><subject>Adenosine Diphosphate - metabolism</subject><subject>Adenosine Triphosphate - metabolism</subject><subject>Adrenergic beta-Antagonists - therapeutic use</subject><subject>Analysis of Variance</subject><subject>Animals</subject><subject>Antianginal agents. Coronary vasodilator agents</subject><subject>Antioxidants - therapeutic use</subject><subject>Biological and medical sciences</subject><subject>Carbazoles - therapeutic use</subject><subject>Cardiovascular system</subject><subject>Carvedilol</subject><subject>Dose-Response Relationship, Drug</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Myocardial Reperfusion Injury - prevention & control</subject><subject>Myocardium - metabolism</subject><subject>Oxidative Stress - drug effects</subject><subject>Perfusion</subject><subject>Pharmacology. Drug treatments</subject><subject>Phosphocreatine - metabolism</subject><subject>Propanolamines - therapeutic use</subject><subject>Propranolol - therapeutic use</subject><subject>Rabbits</subject><subject>Random Allocation</subject><issn>0008-6363</issn><issn>1755-3245</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2000</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpNkNtKxDAQhoMouh4eQcmFiF5UJ02TNN6JeIIFwcN1SNspRtpGk3Zx397WXdSr4Yfvnxk-Qg4ZnDNg8iICQJ5ILvkpwNkU0oRtkBlTQiQ8zcQmmf0iO2Q3xvcxCqGybbLDQEuu0nxGiieshrJ3vqO-pv7LVbZ3C6SxDxgjLZa0tGGBlWt8c0mDb5C6jrbWdT12titxqrlYvllsXUnbpR_5yg0tXThbuMb1y32yVdsm4sF67pHX25uX6_tk_nj3cH01T8osU31S1KismB5E5FpCrSut84KJHKTMdKaVtCxLNfCiAqiVRpRKp7XUuaoEcr5HTlZ7P4L_HDD2ph0fw6axHfohGpWmkDMQIyhWYBl8jAFr8xFca8PSMDCTXPM8mTOTOQNgfuQaNvaO1geGosXqX2tlcwSO14CNpW3qMApy8Y_LZMoA-DegcIIj</recordid><startdate>20000818</startdate><enddate>20000818</enddate><creator>CARGNONI, A</creator><creator>CECONI, C</creator><creator>BERNOCCHI, P</creator><creator>BORASO, A</creator><creator>PARRINELLO, G</creator><creator>CURELLO, S</creator><creator>FERRARI, R</creator><general>Oxford University Press</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>20000818</creationdate><title>Reduction of oxidative stress by carvedilol: role in maintenance of ischaemic myocardium viability</title><author>CARGNONI, A ; CECONI, C ; BERNOCCHI, P ; BORASO, A ; PARRINELLO, G ; CURELLO, S ; FERRARI, R</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c447t-bfe7a55574ee3960f9d998b158066494976a142903bd00f79ee6792f6987d5e33</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2000</creationdate><topic>Adenosine Diphosphate - metabolism</topic><topic>Adenosine Triphosphate - metabolism</topic><topic>Adrenergic beta-Antagonists - therapeutic use</topic><topic>Analysis of Variance</topic><topic>Animals</topic><topic>Antianginal agents. Coronary vasodilator agents</topic><topic>Antioxidants - therapeutic use</topic><topic>Biological and medical sciences</topic><topic>Carbazoles - therapeutic use</topic><topic>Cardiovascular system</topic><topic>Carvedilol</topic><topic>Dose-Response Relationship, Drug</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Myocardial Reperfusion Injury - prevention & control</topic><topic>Myocardium - metabolism</topic><topic>Oxidative Stress - drug effects</topic><topic>Perfusion</topic><topic>Pharmacology. Drug treatments</topic><topic>Phosphocreatine - metabolism</topic><topic>Propanolamines - therapeutic use</topic><topic>Propranolol - therapeutic use</topic><topic>Rabbits</topic><topic>Random Allocation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>CARGNONI, A</creatorcontrib><creatorcontrib>CECONI, C</creatorcontrib><creatorcontrib>BERNOCCHI, P</creatorcontrib><creatorcontrib>BORASO, A</creatorcontrib><creatorcontrib>PARRINELLO, G</creatorcontrib><creatorcontrib>CURELLO, S</creatorcontrib><creatorcontrib>FERRARI, R</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Cardiovascular research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>CARGNONI, A</au><au>CECONI, C</au><au>BERNOCCHI, P</au><au>BORASO, A</au><au>PARRINELLO, G</au><au>CURELLO, S</au><au>FERRARI, R</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Reduction of oxidative stress by carvedilol: role in maintenance of ischaemic myocardium viability</atitle><jtitle>Cardiovascular research</jtitle><addtitle>Cardiovasc Res</addtitle><date>2000-08-18</date><risdate>2000</risdate><volume>47</volume><issue>3</issue><spage>556</spage><epage>566</epage><pages>556-566</pages><issn>0008-6363</issn><eissn>1755-3245</eissn><coden>CVREAU</coden><abstract>To differentiate the impact of the beta-blocking and the anti-oxidant activity of carvedilol in maintaining myocardium viability.
Isolated rabbit hearts, subjected to aerobic perfusion, or low-flow ischaemia followed by reperfusion, were treated with two doses of carvedilol, one dose (2.0 microM) with marked negative inotropic effect due to beta-blockage and the other (0.1 microM) with no beta-blockage nor negative inotropism. Carvedilol was compared with two doses of propranolol, 1.0 - without - and 5.0 microM - with negative inotropic effect. Anti-oxidant activity was measured as the capacity to counteract the occurrence of oxidative stress and myocardium viability as recovery of left ventricular function on reperfusion, membrane damage and energetic status.
Carvedilol counteracted the ischemia and reperfusion induced oxidative stress: myocardial content of reduced glutathione, protein and non-protein sulfhydryl groups after ischaemia and particularly after reperfusion, was higher in hearts treated with carvedilol, while the myocardial content of oxidised glutathione was significantly reduced (0.30+/-0.03 and 0.21+/-0.02 vs. 0.39+/-0.03 nmol/mg prot, both P<0.01, in 0.1 and 2.0 microM). At the same time, carvedilol improved myocardium viability independently from its beta-blocking effect. On the contrary, propranolol maintained viability only at the higher dose, although to a lesser extent than carvedilol. This suggests that the effects of propranolol are dependent on energy saving due to negative inotropism. The extra-protection observed with carvedilol at both doses is likely due to its anti-oxidant effect.
Our data show that the anti-oxidant activity of carvedilol is relevant for the maintenance of myocardium viability.</abstract><cop>Oxford</cop><pub>Oxford University Press</pub><pmid>10963728</pmid><doi>10.1016/s0008-6363(00)00082-1</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Cardiovascular research, 2000-08, Vol.47 (3), p.556-566 |
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| source | MEDLINE; Oxford Journals Online; Alma/SFX Local Collection; EZB Electronic Journals Library |
| subjects | Adenosine Diphosphate - metabolism Adenosine Triphosphate - metabolism Adrenergic beta-Antagonists - therapeutic use Analysis of Variance Animals Antianginal agents. Coronary vasodilator agents Antioxidants - therapeutic use Biological and medical sciences Carbazoles - therapeutic use Cardiovascular system Carvedilol Dose-Response Relationship, Drug Male Medical sciences Myocardial Reperfusion Injury - prevention & control Myocardium - metabolism Oxidative Stress - drug effects Perfusion Pharmacology. Drug treatments Phosphocreatine - metabolism Propanolamines - therapeutic use Propranolol - therapeutic use Rabbits Random Allocation |
| title | Reduction of oxidative stress by carvedilol: role in maintenance of ischaemic myocardium viability |
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